The interaction between ferroptosis and inflammatory signaling pathways

Cell Death and Disease, Год журнала: 2023, Номер 14(3)

Опубликована: Март 21, 2023

Abstract Ferroptosis is an iron-dependent regulated cell death driven by excessive lipid peroxidation. Inflammation one common and effective physiological event that protects against various stimuli to maintain tissue homeostasis. However, the dysregulation of inflammatory responses can cause imbalance immune system, dysfunction death. Recent studies have pointed out activation inflammation, including multiple inflammation-related signaling pathways, lead ferroptosis. Among related signal transduction we focused on five classical namely, JAK-STAT, NF-κB, inflammasome, cGAS-STING MAPK expounded their roles in To date, many agents shown therapeutic effects ferroptosis-related diseases modulating aforementioned pathways vivo vitro. Moreover, regulatory these iron metabolism peroxidation been described detail, contributing further understanding pathophysiological process Taken together, targeting inflammation will provide appropriate ways intervene ferroptosis diseases.

Язык: Английский

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Molecular mechanisms of ferroptosis and their involvement in brain diseases

Pharmacology & Therapeutics, Год журнала: 2023, Номер 244, С. 108373 - 108373

Опубликована: Март 8, 2023

Ferroptosis is a type of regulated cell death characterized by intracellular accumulation iron and reactive oxygen species, inhibition system Xc-, glutathione depletion, nicotinamide adenine dinucleotide phosphate oxidation lipid peroxidation. Since its discovery characterization in 2012, many efforts have been made to reveal the underlying mechanisms, modulating compounds, involvement disease pathways. inducers include erastin, sorafenib, sulfasalazine glutamate, which, inhibiting prevent import cysteine into cells. RSL3, statins, Ml162 Ml210 induce ferroptosis peroxidase 4 (GPX4), which responsible for preventing formation peroxides, FIN56 withaferin trigger GPX4 degradation. On other side, inhibitors ferrostatin-1, liproxstatin-1, α-tocopherol, zileuton, FSP1, CoQ10 BH4, interrupt peroxidation cascade. Additionally, deferoxamine, deferiprone N-acetylcysteine, targeting cellular pathways, also classified as inhibitors. Increased evidence has established distinct brain diseases, including Alzheimer's, Parkinson's Huntington's amyotrophic lateral sclerosis, multiple Friedreich's ataxia. Thus, deep understanding how contributes these it can be modulated, open new window opportunities novel therapeutic strategies targets. Other studies shown sensitivity cancer cells with mutated RAS induction that chemotherapeutic agents synergize tumor treatment. tempting consider may arise target mechanistic pathway treatment tumors. Therefore, this work provides an up-to-date review on molecular mechanisms their diseases. In addition, information main targets provided.

Язык: Английский

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Molecular mechanisms of ferroptosis and relevance to inflammation

Inflammation Research, Год журнала: 2022, Номер 72(2), С. 281 - 299

Опубликована: Дек. 19, 2022

Язык: Английский

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Polystyrene microplastics up-regulates liver glutamine and glutamate synthesis and promotes autophagy-dependent ferroptosis and apoptosis in the cerebellum through the liver-brain axis

Environmental Pollution, Год журнала: 2022, Номер 307, С. 119449 - 119449

Опубликована: Май 9, 2022

Язык: Английский

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Ferroptosis: regulation by competition between NRF2 and BACH1 and propagation of the death signal

FEBS Journal, Год журнала: 2022, Номер 290(7), С. 1688 - 1704

Опубликована: Фев. 2, 2022

Ferroptosis is triggered by a chain of intracellular labile iron-dependent peroxidation cell membrane phospholipids. important not only as cause ischaemic and neurodegenerative diseases but also mechanism cancer suppression, better understanding its regulatory required. It has become clear that ferroptosis finely controlled two oxidative stress-responsive transcription factors, NRF2 (NF-E2-related factor 2) BACH1 (BTB CNC homology 1). inhibit promote ferroptosis, respectively, activating or suppressing the expression genes in major pathways ferroptosis: iron metabolism, GSH (glutathione) -GPX4 (glutathione peroxidase 4) pathway FSP1 (ferroptosis suppressor protein 1)-CoQ (coenzyme Q) pathway. In addition to this, control through regulation lipid metabolism differentiation. This multifaceted considered have been acquired during evolution multicellular organisms, allowing utilization for maintaining homeostasis, including suppression. terms cell-cell interaction, it revealed property propagating surrounding cells along with peroxidation. The propagation phenomenon could be used realize anticancer therapy future. this review, these points will summarized discussed.

Язык: Английский

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Pharmacological Inhibition of Ferroptosis as a Therapeutic Target for Neurodegenerative Diseases and Strokes

Advanced Science, Год журнала: 2023, Номер 10(24)

Опубликована: Июнь 21, 2023

Emerging evidence suggests that ferroptosis, a unique regulated cell death modality is morphologically and mechanistically different from other forms of death, plays vital role in the pathophysiological process neurodegenerative diseases, strokes. Accumulating supports ferroptosis as critical factor diseases strokes, pharmacological inhibition therapeutic target for these diseases. In this review article, core mechanisms are overviewed roles strokes described. Finally, emerging findings treating through This demonstrates by bioactive small-molecule compounds (ferroptosis inhibitors) could be effective treatments highlights potential promising avenue used to prevent article will shed light on developing novel regimens slow down progression future.

Язык: Английский

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Targeting epigenetic and posttranslational modifications regulating ferroptosis for the treatment of diseases

Signal Transduction and Targeted Therapy, Год журнала: 2023, Номер 8(1)

Опубликована: Дек. 10, 2023

Abstract Ferroptosis, a unique modality of cell death with mechanistic and morphological differences from other modes, plays pivotal role in regulating tumorigenesis offers new opportunity for modulating anticancer drug resistance. Aberrant epigenetic modifications posttranslational (PTMs) promote resistance, cancer progression, metastasis. Accumulating studies indicate that can transcriptionally translationally determine vulnerability to ferroptosis functions as driver nervous system diseases (NSDs), cardiovascular (CVDs), liver diseases, lung kidney diseases. In this review, we first summarize the core molecular mechanisms ferroptosis. Then, roles processes, including histone PTMs, DNA methylation, noncoding RNA regulation such phosphorylation, ubiquitination, SUMOylation, acetylation, ADP-ribosylation, are concisely discussed. The PTMs genesis cancers, NSD, CVDs, well application PTM modulators therapy these then discussed detail. Elucidating mediated by will facilitate development promising combination therapeutic regimens containing or PTM-targeting agents inducers be used overcome chemotherapeutic resistance could prevent addition, highlight potential approaches chemoresistance halt

Язык: Английский

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Srs11‐92, a ferrostatin‐1 analog, improves oxidative stress and neuroinflammation via Nrf2 signal following cerebral ischemia/reperfusion injury

CNS Neuroscience & Therapeutics, Год журнала: 2023, Номер 29(6), С. 1667 - 1677

Опубликована: Фев. 27, 2023

Ferroptosis is increasingly becoming to be considered as an important mechanism of pathological cell death during stroke, and specific exogenous ferroptosis inhibitors have the ability reverse cerebral ischemia/reperfusion injury. However, research on Srs11-92 (AA9), a ferrostatin-1 (Fer-1) analog, in preclinical studies limited.In middle artery occlusion-reperfusion (MCAO/R) mice model or oxygen-glucose deprivation/reperfusion (OGD/R) model, Fer-1, AA9, and/or ML385 were administered, brain infarct size, neurological deficits, neuronal damage, oxidative stress, neuroinflammation determined after vitro vivo.Fer-1 AA9 improved deficits MCAO/R, inhibited overloaded iron deposition, ROS accumulation, response: it also increased expression GPx4, Nrf2, HO-1 suppressed HMGB1 NF-κB p65 epicenter injured hippocampal formation. Nrf2 inhibitor reversed neuroprotective effect including stress neuroinflammation. In showed that relieved OGD/R-induced via pathway, which was impaired by primary neurons.The findings imply Fer-1 analog may suitable for further translational protection damage signal pathway-mediated stroke others diseases.

Язык: Английский

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Research on ferroptosis as a therapeutic target for the treatment of neurodegenerative diseases

Ageing Research Reviews, Год журнала: 2023, Номер 91, С. 102035 - 102035

Опубликована: Авг. 23, 2023

Ferroptosis is an iron- and lipid peroxidation (LPO)-mediated programmed cell death type. Recently, mounting evidence has indicated the involvement of ferroptosis in neurodegenerative diseases, especially Alzheimer's disease (AD), Parkinson's (PD), multiple sclerosis (MS), amyotrophic lateral (ALS), Huntington's (HD), so on. Treating presents opportunities as well challenges for diseases. This review provides a comprehensive overview underlying mechanisms that contribute to occurrence ferroptosis, their implications pathogenesis advancement major disorders. Meanwhile, we summarize interaction between other types diseases contribution corresponding drug development. In addition, specifically recent advances developing therapeutic means targeting these which may guide future approaches effective management devastating medical conditions.

Язык: Английский

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Co-exposure to environmentally relevant concentrations of cadmium and polystyrene nanoplastics induced oxidative stress, ferroptosis and excessive mitophagy in mice kidney

Environmental Pollution, Год журнала: 2023, Номер 333, С. 121947 - 121947

Опубликована: Июнь 1, 2023

Язык: Английский

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